Hepatobiliary & Muscle II Flashcards

Dr. Parsley

1
Q

What are the 3 main categories (causes) for hyperbilirubinemia?

A

pre-hepatic
hepatic
post-hepatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is hyperbilirubinemia - pre-hepatic?

A

increased production of bilirubin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is hyperbilirubinemia - hepatic?

A

decreased hepatic uptake or secretion of bilirubin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is hyperbilirubinemia - post-hepatic?

A

post-hepatic obstruction of bile flow (cholestasis) —> reflux of bilirubin into blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Look at this picture on how bilirubin is produced

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where is bilirubin conjugated?

A

hepatocyte in the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Where is the red blood cell phagocytosed and breakdown of hemoglobin occurs to produce bilirubin?

A

macrophage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the products of hemoglobin? Where does this occur?

A

heme —> biliverdin & iron —> from biliverdin comes bilirubin
globin

red blood cell - pictures is showing the spleen specifically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Unconjugated bilirubin is transported with ______ in the blood

A

albumin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Conjugated bilirubin (Bc) is transported from the hepatocyte to _____

A

canaliculi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Elaborate on hyperbilirubinemia - pre-hepatic and why it leads to this

A

hemolysis: unconjugated bilirubin > conjugated

rate of bilirubin formation exceeds liver’s capacity for uptake/excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Elaborate on hyperbilirubinemia - hepatic and why it leads to this

A

decreased in liver functional mass

can’t get it out; converted to conjugated (intra-hepatic cholestasis)

functional cholestasis: conjugated greater than unconjugated: typically little to no ALP, but GGT high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Elaborate on hyperbilirubinemia - post-hepatic and why it leads to this

A

extra-hepatic cholestasis: conjugated greater than unconjugated

liver can conjugate but can’t excrete

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do you assess bilirubin?

A

total bilirubin (Bt)

direct: conjugated
indirect: unconjugated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is decreased liver functional mass also called?

A

hepatic insufficiency
“liver failure” —> be careful saying

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the confusion with a decrease in liver functional mass?

A
17
Q

How do you assess hepatic function?

A
18
Q

At what percentage of lost functional mass do liver products decrease?

A

70% - decrease is non-specific

19
Q

What levels are glucose and globulins when testing for decreased functional mass?

A

glucose: can be elevated (low in fasting animals)

globulins: can be decreased because liver isn’t making globulins

20
Q

Define a congenital PSS

A

portal vein hypoperfusion can result in secondary loss in functional mass

21
Q

Define an acquired PSS

A

can be secondary to chronic liver disease / decrease in hepatic functional mass

22
Q

What would you expect to be increased with a PSS?

A

ammonia
bile acids

= evidence of decreased hepatic functional mass

(liver filters toxins but if not? delivered directly to systemic blood)

23
Q

Contrast congenital vs. acquired shunts?

A
24
Q

Describe ammonia metabolism

A

produced by the GI microbes

transported to the liver
- made into urea
- goes into blood (BUN)
- excreted by the kidney

25
Q

What are your differentials with hyperammonemia?

A
  • decrease in hepatic functional mass
    > decrease uptake and conversion of NH3 to urea
  • PSS - NH3 bypasses the lvier
  • feed additive in ruminants
  • intestinal disease in horse
  • unfasted sample
26
Q

How do you handle ammonia?

A

has special handling requirements

27
Q

Who makes bile acids?

A

hepatocytes

28
Q

Trace the production and circulation of bile acids

A

made by hepatocytes —> delivered to intestine (via bile duct) —> absorbed by portal circulation —> liver —> re-excreted —> bile (enterohepatic circulation)

29
Q

What are some differentials for increased bile acids?

A
  • decrease in hepatic functional mass
  • PSS
  • cholestasis (do NOT run bile acids)
  • false (physiologic elevation)
    > gallbladder contraction elevates fasting bile acids
30
Q

What are some differentials for decreased bile acids?

A

GI disease (abnormal motility or malabsorption)

31
Q

What do you expect with simultaneous liver insufficiency and GI malabsorption?

A

can balance out

32
Q

What are some species differences between small and large animals - bile acids?

A
33
Q

What is the sequela to decreased hepatic function?

A
34
Q

What is going on here? 8 year old FS Doberman with chronically increased ALT and AST

A

chronic liver injury

35
Q

7 month old MI retriever presented for lethargy, poor weight gain, and now the owner has noted what they think looked like a seizure.

Which of these is most likely to cause the chemistry abnormalities?
a) Amanita mushroom toxicosis
b) Congenital PSS
c) Cholelithiasis
d) Bacterial septicemia

A

b) Congenital PSS

36
Q

12 month MI beagle presented for PUPD and an enlarged abdomen

A

Acquired PSS

37
Q

What fraction of bilirubin enters urine?

A

very little or none